KRAS mutation

P=N/A, N=150, Active, not recruiting, BAIYONG SHEN | Enrolling by invitation --> Active, not recruiting | Trial completion date: Nov 2025 --> Aug 2028 | Trial primary completion date: Nov 2025 --> Jan 2028

P2, N=30, Recruiting, Ryan Gentzler, MD | Trial completion date: Aug 2028 --> Feb 2028 | Trial primary completion date: Mar 2026 --> Feb 2027

P1, N=91, Terminated, Deciphera Pharmaceuticals, LLC | Phase classification: P1/2 --> P1 | N=144 --> 91 | Trial completion date: Aug 2028 --> Mar 2026 | Active, not recruiting --> Terminated | Trial primary completion date: Aug 2027 --> Mar 2026; Trial terminated due to business decision, not based on any safety or efficacy concerns.

DOG1-positive CAFs were associated with better overall survival. This study suggests that DOG1 expression is detected in a high proportion of CRC because it is expressed in neoplastic cells of various histological subtypes of CRC that secrete gel-forming mucins, independently of mucinous features or in CAFs of conventional adenocarcinomas.

Foundation model-based scoring produces expert-level, scalable biomarker quantification. The resulting TME phenotypes - TROP-2-high immune-deserted vs cMET-high, immune-active - reveal therapeutic implications for combining ADCs with immunotherapies or kinase inhibitors.

A comprehensive assessment of the post-treatment tumor microenvironment revealed that KRAS degradation increased tumor-derived CCL5 levels, thereby promoting CD8+ T-cell recruitment and amplifying antitumor responses. Thus, AUTACE represents a promising strategy for the treatment of KRAS/TP53 co-mutant tumors.

Mechanistically, we demonstrate induction of senescence following HUWE1 depletion - characterised by impaired proliferation, an atypical cell cycle distribution, emergence of morphologically abnormal enlarged cells, increased β-galactosidase activity, and transcriptional reprogramming associated with inflammatory senescence-associated secretory phenotype (SASP) signalling and NFκB activation. Together, these data highlight a crucial role for HUWE1 in mutant Kras-induced LUAD tumorigenesis and in the continued growth and proliferation of established LUAD cells, confirming HUWE1 as a rational therapeutic target for LUAD.

Taken together, the results highlight the importance of targeting different metabolites and metabolic pathways in cancer therapy.   Cite this article as: K.ker ŞC, Tura.lı İD. Dependency of non-small cell lung cancer (NSCLC) cells on glutamine and glucose levels in the presence of metformin. Eurasian J Med. 2026, 58(2), 1018, doi:10.5152/eurasianjmed.2026.251018.

Recent breakthroughs with next-generation KRAS inhibitors have transformed the therapeutic landscape for pancreatic cancer. This review synthesizes evidence from basic research and clinical translation to provide a theoretical foundation and practical guidance for the precision treatment of KRAS-mutant pancreatic cancer.

N+T in patients with HER2-mutant metastatic TNBC appeared to prolong responses versus neratinib alone, representing a novel approach for biomarker-defined metastatic TNBC patients. Based on these and previously published data, neratinib-based combinations are endorsed by NCCN guidelines for patients with hormone receptor-positive or -negative metastatic breast cancer with activating HER2 mutations.

P=N/A, N=102, Completed, Amgen | Recruiting --> Completed | Trial completion date: Jun 2026 --> Dec 2025

P1, N=101, Recruiting, Suzhou Abogen Biosciences Co., Ltd. | Not yet recruiting --> Recruiting